Abstract Alzheimer's disease (AD) is the most common cause of dementia leading to irreversible neurodegeneration and cognitive decline. Despite extensive efforts and numerous clinical trials of potential disease-modifying therapies, there is yet no effective way to cure or prevent this disease. The core pathological hallmarks of AD are extracellular deposits of the aggregated Aβ42 protein (amyloid plaques) and intracellular aggregates of hyper-phosphorylated tau (neurofibrillary tangles). It is well established that defective autophagy in neuronal cells contribute to disease pathology in AD. Autophagy is a physiological process and conserved degradation pathway which is involved in the basal turnover of long-lived proteins and organelles. Several studies demonstrated that autophagy plays an important role in amyloid clearance from the brain and that impaired autophagy contribute to amyloid aggregation in AD brains. It is well accepted now that deterioration of autophagy activity precedes the accumulation of Aβ42 and neuronal loss. In this project we will explore the usage of a new marker for dysfunctional autophagy in AD.